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Serotonin and motherhood: From molecules to mood.
Pawluski JL, Li M, Lonstein JS (2019) Serotonin and motherhood: From molecules to mood. Front Neuroendocrinol 53:100742. doi: 10.1016/j.yfrne.2019.03.001
Summary: Serotonin may affect how mothers perceive or behaviorally readjust to changes in the sensory cues emitted by their offspring as they age. The DR serotonin-lesioned mothers studied by Holschbach and colleagues (2018) were much less maternally aggressive, which was concomitant with reduced serotonin-immunoreactive fiber density in the anterior hypothalamus, a brain site previously implicated in serotonin’s influence on aggressive behaviors in male animals.
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Inhibition of methamphetamine self-administration and reinstatement by central blockade of angiotensin II receptor in rats.
Xu X, Pan J, Li X, Cui Y, Mao Z, Wu B, Xu H, Zhou W, Liu Y (2019) Inhibition of methamphetamine self-administration and reinstatement by central blockade of angiotensin II receptor in rats. J Pharmacol Exp Ther 369(2):244-258. doi: 10.1124/jpet.118.255729 PMID: 30867225
Objective: To explore the role of central angiotensin II receptor (ATR) in drug taking and seeking behavior associated with methamphetamine (METH) use disorder.
Summary: The AT1R-PLCβ-CREB signaling pathway was found to be associated with the effect of AT1R on the drug-taking and drug-seeking behavior involving METH use disorder.
Usage: Membranes were incubated at 4°C overnight (1:1000). Western blot.
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Knockdown of fidgetin improves regeneration of injured axons by a microtubule-based mechanism.
Matamoros AJ, Tom VJ, Wu D, Rao Y, Sharp DJ, Baas PW (2019) Knockdown of fidgetin improves regeneration of injured axons by a microtubule-based mechanism. J Neurosci 39(11):2011-2024. doi: 10.1523/JNEUROSCI.1888-18.2018 PMID: 30647150
Objective: To test whether fidgetin knockdown assists axonal regeneration.
Summary: Results show that DRG neurons in which fidgetin was knocked down displayed enhanced regeneration of axons across the dorsal root entry zone into the spinal cord. The results establish fidgetin as a novel therapeutic target to augment nerve regeneration.
Usage: immunohistochemistry
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Cholinergic deficit induced by central administration of 192IgG-Saporin is associated with activation of microglia and cell loss in the dorsal hippocampus of rats
Dobryakova YV, Volobueva MN, Manolova AO, Medvedeva TM, Kvichansky AA, Gulyaeva NV, Markevich VA, Stepanichev MY, Bolshakov AP (2019) Cholinergic deficit induced by central administration of 192IgG-Saporin is associated with activation of microglia and cell loss in the dorsal hippocampus of rats. Front Neurosci 13:146. doi: 10.3389/fnins.2019.00146
Objective: To study the histopathology of the hippocampus and the responses of microglia and astrocytes using immunohistochemistry and neuroglial gene expression.
Summary: Cholinergic degeneration in the medial septal area induced by intracerebroventricular administration of 192IgG-saporin results in an increase in the number of microglial cells and neuron degeneration in the dorsal hippocampus.
Usage: 192-IgG-SAP was injected bilaterally into both ventricles (i.c.v.) at a dose of 4 μg/site.
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Spinal α2-adrenoceptors and neuropathic pain modulation; therapeutic target.
Bahari Z, Meftahi GH (2019) Spinal α2-adrenoceptors and neuropathic pain modulation; therapeutic target. Br J Pharmacol 176(14):2366-2381. doi: 10.1111/bph.14580
Objective: To provide an an overview of the cellular mechanisms through which brainstem adrenergic descending inhibitory processing can alter spinal pain transmission to the higher centres, and how these pathways change in neuropathic pain conditions focusing on the role of spinal α2‐adrenoceptors in the spinal dorsal horn.
Summary: The α2‐adrenoceptor agonist may be useful to treat neuropathic pain.
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Noradrenergic terminals are the primary source of α2-adrenoceptor mediated dopamine release in the medial prefrontal cortex.
Devoto P, Flore G, Saba P, Scheggi S, Mulas G, Gambarana C, Spiga S, Gessa GL (2019) Noradrenergic terminals are the primary source of α2-adrenoceptor mediated dopamine release in the medial prefrontal cortex. Prog Neuropsychopharmacol Biol Psychiatry 90:97-103. doi: 10.1016/j.pnpbp.2018.11.015
Objective: To clarify the relative contribution of dopamine (DA) release from noradrenergic and dopaminergic terminals to DA output induced by blockade of α2-adrenoreceptors and the norepinephrine transporter.
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Palladium based nanoparticles for the treatment of advanced melanoma.
Elsey J, Bubley JA, Zhu L, Rao S, Sasaki M, Pollack BP, Yang L, Arbiser JL (2019) Palladium based nanoparticles for the treatment of advanced melanoma. Sci Rep 9:3255. doi: 10.1038/s41598-019-40258-6 PMID: 30824801
Usage: immunohistochemistry (1:300)
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Combining naproxen and a dual amylin and calcitonin receptor agonist improves pain and structural outcomes in the collagen-induced arthritis rat model.
Katri A, Dąbrowska A, Löfvall H, Ding M, Karsdal MA, Andreassen KV, Thudium CS, Henriksen K (2019) Combining naproxen and a dual amylin and calcitonin receptor agonist improves pain and structural outcomes in the collagen-induced arthritis rat model. Arthritis Res Ther 21(1):68. doi: 10.1186/s13075-019-1819-9 PMID: 30795801
Objective: To investigate if combining a standard of care NSAID (naproxen) with a Key Bioscience peptides (KBP) resulted in improvement in pain scores, as well as disease activity and structural damage in a rat model of rheumatoid arthritis (RA).
Summary: Combination therapy had improved efficacy over naproxen monotherapy; combination therapy resulted in improved health scores, and reduced mechanical and cold allodynia assessment. Furthermore, protection of articular cartilage structure and preservation of bone structure and bone volume were also observed.
Usage: histology (1:4000)
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Degeneration of ipRGCs in mouse models of huntington’s disease disrupts non-image-forming behaviors before motor impairment.
Lin M-S, Liao P-Y, Chen H-M, Chang C-P, Chen S-K, Chern Y (2019) Degeneration of ipRGCs in mouse models of huntington’s disease disrupts non-image-forming behaviors before motor impairment. J Neurosci 39(8):1505. doi: 10.1523/JNEUROSCI.0571-18.2018 PMID: 30587542
Summary: Results show that M1 ipRGCs were susceptible to the toxicity caused by mutant Huntingtin. The resultant impairment of M1 ipRGCs contributed to the early degeneration of the ipRGC–SCN pathway and disrupted circadian regulation during HD progression.
Usage: Immunostaining (1:3000)
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Sacituzumab for the treatment of triple-negative breast cancer: the poster child of future therapy?
Zangardi ML, Spring LM, Nagayama A, Bardia A (2019) Sacituzumab for the treatment of triple-negative breast cancer: the poster child of future therapy?. Expert Opin Investig Drugs 28(2):107-112. doi: 10.1080/13543784.2019.1555239 PMID: 30507322
Summary: This publication explores the potential of sacituzumab as a treatment for triple-negative breast cancer, highlighting its promising role as a leading candidate for future therapeutic approaches. The study suggests that sacituzumab may represent a breakthrough in the management of this aggressive breast cancer subtype, raising hopes for improved outcomes in patients.